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USMLE STEP 1 > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

The information from this deck should be pulled from: Netter's Physiology USMLE Review Book BRE review Book Lecture MNTS from 2016

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USMLE® Step 1 flashcards
1
Q

Pulmonary hypertension

A

Right ventricular hypertrophy occurs in response to heightened pressure in the lungs

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2
Q

Aortic stenosis

A

Narrowing of the aortic valve that results in left ventricle hypertrophy

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3
Q

Mitral incompetence

A

Left atrial dilation may develop as a result of the elevation of left atrial pressure and volume caused by mitral regurgitation

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4
Q

What is the pulmonary arterial pressure?

A

25/10 (mean pressure 15)

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5
Q

What aortic pressure?

A

120/80 (mean pressure 95)

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6
Q

What is the volume distribution in the blood of the body?

A

64% veins 9% lungs 8% small arteries & arterioles 7% large arteries 7% heart in diastole 5% capillaries

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7
Q

What is the distribution of vascular resistance?

A

47% arterioles 27% capillaries 19% large arteries 7% veins

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8
Q

What is the distribution of blood flow in the body?

A

24% liver and GI 21% skeletal muscle 20% kidney 18% skin and other organs 13% brain 4% heart

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9
Q

What is VO2 distribution of blood flow in the body?

A

27% skeletal 23% liver and GI 21% brain 11% skin and other organs 11% heart 7% kidney

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10
Q

What is the resting membrane potential of the SA node?

A

-60mV

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11
Q

What is a normal rate of the SA node?

A

70 bpm

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12
Q

What are the phases of the action potentials of myocytes and His-Purkinje fiber?

A

Phase 4 (resting membrane potential): Close to the Nernst potential for K because of the efflux of K. Ion levels are restored by the Na/K pump, the Na/Ca exchanger, and the ATP-dependent Ca pump. Phase 0 (upstroke of the action potential): When cells reach threshold, Na ion gated channels open coupled with reduced conductance of K current. This depolarizes the cell. Phase 1 (rapid repolarization to the plateau): Na channel are inactivated and voltage gated K channels are opened. Phase 2 (the plateau): Slow L type Ca channels and inward current of Ca moderates the effects of the outflow of K. Phase 3 (repolarization): Gradual inactivation of the L-type Ca channels leads to activation of K channels causing rapid depolarization.

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13
Q

Effective refractory period

A

Phase 1 to much of phase 3, during which an AP cannot be generated

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14
Q

Relative refractory period

A

Until membrane potential is restored, an AP can be generated but it is more difficult

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15
Q

Chronotropic

A

effects heart rate

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16
Q

Dromotropic

A

effects conduction velocity

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17
Q

Inotropic

A

effects myocardial contractility

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18
Q

What effect does the sympathetic nervous system have on chromotoropic, dromotropic, and inotropics?

A

Increases them

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19
Q

What effect does the parasympathetic nervous system have on chromotoropic, dromotropic, and inotropics

A

Decreases them

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20
Q

P wave

A

atrial depolarization

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21
Q

QRS complex

A

ventricular depolarization

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22
Q

T wave

A

ventricular repolarization

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23
Q

Bradycardia

A

resting heart rate below 60 bpm

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24
Q

Tachycardia

A

resting heart rate above 100 bpm

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25
Q

First degree AV block

A

Delay in conduction through the AV node. Thus, there is an extended PR interval with normal sinus rhythm.

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26
Q

Normal PR interval

A

0.20 s

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27
Q

Second degree AV block

A

Delay in conduction through the AV node that sometimes does not result in a QRS complex. This may be produced by ischemia or infarction.

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28
Q

Third degree AV block

A

Complete blockage of the AV node. P waves are dissociated from the QRS complexes with an escape pacemaker below the AV node with a rate of 40-55 bpm which is partially responsive to the sympathetics. When the block is below in the bundle of His, the escape rhythm is 20-40 bpm which can be insufficient even at rest. Usually a pacemaker is put in at this point.

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29
Q

Describe action potential of pacemaker cells (SA node cells)

A

ADD INFO!

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30
Q

Describe the pathway of the electrical charge through the heart.

A

SA node –> AV node –> bundle of his –> bundle branchs fiber –> Purkinje fibers –> ventricular muscle

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31
Q

U wave

A

Occurs in 50-70% of people following the T wave.

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32
Q

Equation for rate of flow

A

Q = change in pressure/resistance Q = P/R

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33
Q

Systolic arterial pressure

A

peak arterial pressure reached at point of ejective of blood by heart, usually 120

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34
Q

Diastolic arterial pressure

A

lowest arterial pressure reached during diastole, usually 80

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35
Q

Arterial pulse pressure

A

Systolic pressure - diastolic pressure depends on the stroke volume

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36
Q

Mean arterial pressure

A

average pressure over a complete cardiac cycle of systole and diastole dependent on peripheral resistance and cardiac output MAP = 1/3(pulse pressure) + diastolic pressure

NB: Pulse pressure is the difference between diastolic and systolic pressure

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37
Q

What factors impact arterial pressure?

A

arterial compliance, cardiac output, stroke volume, peripheral resistance

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38
Q

Dichrotic notch

A

irregular notch in the descending slop of the arterial pressure curve representing when the aortic valves close

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39
Q

Pressure right ventricle

A

25/0

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40
Q

Pressure left ventricle

A

125/0

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41
Q

Poiseuille’s law

A

Q = P(pi)r^4/n8L (n = viscosity) Flow is… directly: pressure gradient, radius indirectly: viscosity, length

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42
Q

What is the most important factor that influences flow?

A

The radius of the tube because that value is raised to the fourth power.

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43
Q

Sounds of Korotkoff

A

pulsatile sounds heard during blood pressure readings

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44
Q

Pulmonary capillary wedge pressure

A

Venous catheter is passed from veins, right atrium, and right ventricles. We cannot measure the pulmonary venous pressure directly nor the left atria pressure, so the wedge pressure is used. Swan-Gatz catheters have an inflated balloon at the end. Vascular pressure beyond the occlusion equilibrates with downstream pressure and wedge pressure is an indicator of pulmonary venous pressure and left atrial pressure.

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45
Q

Left atrial pressure

A

15/0

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46
Q

Contrast pulse pressures throughout the body.

A

Left atria: 15 Left ventricle: 125 Aorta: 40 Large arteries: 60 Capillaries & veins: 0 Right atrium: 5 Right ventricle: 25

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47
Q

Right ventricle pressure

A

25/0

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48
Q

Resistance equation

A

R = n8L/(pi)r^4 directly: length, viscosity indirectly: radius

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49
Q

Flow equation

A

Q = VA

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50
Q

Laminar flow

A

greatest velocity of flow in the center of the vessel, R below 2000

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51
Q

Reynold’s Number (R)

A

R = VDd/n V = velocity D = diameter d = density n = viscosity

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52
Q

Turbulent flow

A

Flow promoted by high velocity of blood flow, large vessel diameter, low viscosity of blood, abrupt changes in vessel diameter, and vascular branching points; R above 3000; associated with murmurs

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53
Q

Wall tension

A

force necessary to hold together a slit in a vessel’s wall

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54
Q

Leplace’s law

A

T = Pr P = intramural pressure, difference between pressure inside and outside the vessel r = radius

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55
Q

Aortic aneurysm

A

Enlargement of the aorta caused by a weakness in the aorta.

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56
Q

Left heart valves sequence

A

Mitral closure, aortic opening, aortic closing, mitral opening

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57
Q

Right heart valves sequence

A

Tricuspid closure, pulmonic opening, pulmonic closure, tricuspid opening

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58
Q

Aggregate sequence of valves

A

Mitral valve closure, tricuspid closure, pulmonic opening, aortic opening, aortic closure, pulmonic closure, tricuspid opening, mitral opening

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59
Q

What causes the asynchrony between the right and left valves?

A

Pressure gradient between the sides of circulation.

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60
Q

Cardiac output

A

CO = HR x SV normally 5L/min

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61
Q

Cardiac Cycle/ Wiggers Diagram

A

One cycle of ventricular diastole and systole (Map out image)

62
Q

isovolumetric contraction

A

The period during systole when all the valves are shut

63
Q

isovolumetric relaxation

A

The period during diastole when all the valves are shut

64
Q

dicrotic notch

A

A high frequency deflection in the aortic pressure curve when the aortic valve closes

65
Q

Describe the timing of filling the ventricles?

A

By the time of the P wave, most of the blood has filled the ventricles, but the remaining 15% is pushed in with the contraction of the atria.

66
Q

Active ventricular filling

A

The 15% of blood that is pushed into the ventricles by the atrial contraction

67
Q

End diastolic volume (EDV)

A

The volume at the end of diastole with the closure of the mitral valve. (Normal 140 mL)

68
Q

End systolic volume (ESV)

A

The volume at the end of systole with the closure of the aortic valve.

69
Q

Stroke volume

A

EDV - ESV (Normal 70 mL)

70
Q

Rapid passive filling

A

Opening of the mitral valve leads to filling of the ventricles.

71
Q

Slow passive feeling (diastasis)

A

Ventricle fills more slowly because of different pressure differential.

72
Q

A wave

A

Atrial contraction makes this wave

73
Q

C wave

A

During isovolumetric contraction, there is an upward wave in the LAP curve

74
Q

V wave

A

During ejection phase, LAP rises with venous return to the atrium (during mitral valve closure)

75
Q

Why are the venous pulse and the atrial pulse similar?

A

Because there are no valves between the vena cave and right atrium, the atrial pressure curve and venous pulse are similar in shape

76
Q

Phonocardiogram

A

acoustical recording reflecting the heart sounds generated during the cardiac cycle

77
Q

S1

A

closure of mitral and tricuspid valves

78
Q

S2

A

closure of aortic and pulmonic valves

79
Q

What happens during inspiration to S2?

A

During S2, there is a delay causing more filling in the right ventricle due to decreased intrathoracic pressure.

80
Q

S3

A

normal in children, associated with rapid ventricle filling; not heard in normal adults and is a sign of volume overload in congestive heart failure

81
Q

S4

A

active ventricular filling not heard in normal adults

82
Q

How does the autonomic nervous system play a role in regulating cardiac output?

A

The ANS modulates the SA nodal pacemaker rate, myocardial contractility, and vascular smooth muscle tone. Sympathetics - release catecholamines to vessels and heart and a few vascular beds. There is some circulating epinephrine from the adrenal glands as well. Parasympathetics - release Ach to heart and some vascular beds.

83
Q

How is cardiac input regulated in response to a change in posture (standing to lying down)?

A

Increase in venous return –> Increase stroke volume –> increase MAP –> Increase rate of baroreceptor afferent fibers –> increase PNS activity acting on SA node to reduce heart rate and CO –> decrease MAP Increase in venous return –> Increase stroke volume –> increase MAP –> Increase rate of baroreceptor afferent fibers –> decrease sympathetics –> decrease peripheral resistance, decrease venous tones, decrease contractility (decrease stroke volume) –> lower cardiac output –> decrease MAP

84
Q

What mechanisms regulate heart rate?

A

ANS - sympathetics B1 receptor increases cAMP production raising pacemaker and elevation of heart rate; parasympathetics reduce heart rate with Ach Bainbridge reflex response to atrial stretch Thoracic pressure changes during respiration on venous return

85
Q

Respiratory sinus arrythmia

A

Heart rate is increased with inspiration and decreased with expiration.

86
Q

Bainbridge reflex

A

Low-pressure stretch receptors in the atria initiate reflex that increases heart rate through sympathetic nerves

87
Q

Contrast the effects of arterial baroreceptors and atrial baroreceptors.

A

Arterial baroreceptors is a response to regulate arterial pressure and reduces heart rate. Atrial baroreceptors is a response to increase blood volume and increases heart rate.

88
Q

Describe how intravenous infusion can either cause an increased or decreased heart rate depending on the circumstances.

A

When the subject initially had a slow heart rate, with the infusion the Bainbridge reflex will take over and increase the heart rate. However, if the subject had experienced a hemorrhage and had an elevated heart rate, the infusion would result in a decreased heart rate.

89
Q

What parameters is stroke volume dependent on?

A

Preload, afterload, contractility

90
Q

Preload

A

Degree of stretch of myocardial fibers prior to contraction; correlates with EDV; directly related to stroke volume

91
Q

Afterload

A

Force against which the heart has to pump; correlates with arterial pressure or left ventricular pressure during systole; inversely related to stroke volume

92
Q

Contractility (inotropism)

A

Intrinsic ability of cardiac muscle to generate a force at a given fiber length; NOT the same as the force of contraction

93
Q

Frank-Starling relationship

A

An important mechanism for matching cardiac output and venous return and ride and left side cardiac output. An increase in the preload results in an increase in stroke volume and cardiac output. When under sympathetic stimulation, the curve is shifted up and to the left. When under cardiac failure, it gives a lower slope of the curve. In this graph the afterload is assumed to be constant.

94
Q

Cardiac function curve

A

LOOK THIS UP!

95
Q

How does the sympathetic nervous system regulate the stroke volume?

A

Cardiac muscle is directly innervated with sympathetic nerves that release norepinephrine which binds to B1 receptors, increasing intracellular Ca, increasing contractility of the heart. This may also be caused by an increased release of epi by the adrenal medulla.

96
Q

What drugs are used to promote contractility?

A

digitalis, dopamine, and dobutamine

97
Q

Treppe OR Staircase Effect

A

When intervals between cardiac muscle contractions are long, the tension developed is low. There is a stair-like increase in the force of contraction hen frequency (heart rate) is increased. This is associated with an increase in contractility because it is independent from a change in preload. This is associated with higher free intracellular Ca in myocardial fibers.

98
Q

In response to baroreceptor detected fall in arterial pressure, how does cardiac output change?

A

Sympathetics elevate the heart rate; however, this is not effective because the amount of time to fill the heart is smaller so the preload is smaller. By raising the contractility of the heart as well, sympathetics also increase stroke volume. Sympathetic constriction of the venous system elevates the preload of the heart as well.

99
Q

force-velocity relationship

A

Inverse relationship between velocity and maximal contraction. Maximal contraction is when the velocity is 0. Velocity is highest at 0 afterload. Maximum force of contraction occurs at zero velocity, during an isometic contraction.

100
Q

How will the force-velocity relationship change with an increase in preload?

A

Changes in preload result in a family of curves upshifted with the same y-intercept, the same Vm. Vm represents the maximal velocity and corresponds with contractility, so with no change in contractility, the Vm will stay the same. The curve shifts upwards because of the Frank-Starling relationship - greater preload results in greater force of contraction, thus velocity of contraction.

101
Q

How will the force-velocity relationship change with an increase in contractility?

A

This curve will shift up and to the right, thus changing the Vm. Vm is associated with the contractility of the heart. An increased Vm is indicative of a positive ionotropic effect.

102
Q

Ventricular pressure-volume loop

A

A continuous measurement of ventricular volume and ventricular pressure. LOOK THIS IMAGE UP! This can be changed with changes in contractility, preload, and afterload.

103
Q

Ejection fraction

A

Normal >50%

104
Q

What effect will a positive ionotropic drug on ejection fraction?

A

Increase

105
Q

What effect would MI or heart failure have on ejection fraction?

A

Decrease

106
Q

Echocardiogram

A

Sounds are used to produce an image of the heart.

107
Q

How does an increase in stroke volume change a ventricular pressure-volume curve?

A
108
Q

How does an increase in afterload influence pressure voume curves?

A
109
Q

How does an increase in contractility change presssure volume curves?

A
110
Q

What is normal venous return?

A

5L/min; normally it should balance out with cardiac output

111
Q

Compliance

A

Change in volume associated with a change in pressure

112
Q

Orthostatic hypotension

A

decreased blood pressure with standing

113
Q

What is the impact of the baroreceptor reflex on the veins?

A

Constriction of the venous sytem in response to sympathetics prevents the pooling of blood in the extermities.

114
Q

What is the effect of respiration on venous return?

A

During inspiration, the rib cage expands, negative pressure is created in the thorax, diaphragm creates positive pressure in abdomen augmenting return to the thorax

During expiration, the gradient is reduced

115
Q

Vascular function curve

A

Cardiac output is an independent variable on the y-axis and the dependent variable of right atrial pressure is on the x axis.

This is an inverse relationship.

116
Q

Mean circulatory pressure

A

X intercept of the vascular function curve; the pressure at which cardiac output is zero; pressure if the heart stopped beating at the whole blood volume equilibriated

117
Q

Describe a normal curve integrating the vascular and cardiac function curves.

A

ADD IMAGE

118
Q

Describe a normal curve integrating the vascular and cardiac function curves.

A
119
Q

How does a change in volume cahnge vascular and cardiac function curves?

A
120
Q

How does contractility change the vascular and cardiac function curves?

A
121
Q

How does total peripheral resistance influence the vascular and cardiac function curves?

A

Note that MCP stays the same because the volume has remained constant.

122
Q

Tunica intima

A

Innermost layer of endothelial cells; rest on a basement membrane that separates the intima from the media

123
Q

Tunica media

A

Smooth muscle; contractile portion of the vessel

124
Q

Tunica adventitia

A

consists of mainly connective tissue and is the outer layer of vessels

125
Q

Contrast the layers of cells lining vessels for arteries, veins, and capillaries.

A

Arteries: Thick adventitia compared to small arteries (distributing vessels)

Small arteries: Larger media layers (needed for blood flow regulation)

Capillaries: No media or adventitia, single layer of endothelial cells (needed for diffusion)

Veins: circular and longitudinal adventitia (capicitance tubes)

126
Q

Precapillary sphincters

A

Bands of smooth muscle found at the point at which arteries feed into capillaries. These can open and shut to regulate blood flow to capillary beds.

127
Q

Edema

A

swelling with an increase in interstitial fluid

128
Q

vasa vasora

A

Own vascular supply of arteries

129
Q

internal and external elastic membranes

A

bind the tunica media of arteries

130
Q

In general, how is blood flow regulated?

A

change in resistance, flow, or cardiac output

131
Q

Describe how vasodilators act to regulate vascular tone of endothelial cells?

A
132
Q

What are vasodilators?

A

nitrous oxide, prostacylcin

133
Q

What factors stimulate the release of vasodilators?

A

Sheer stress, histamine, Ach, bradykinin, purigenics (ATP)

134
Q

What is the chemical reaction of NO?

A

NO acts on guanalyn cyclase, elevating GMP, cGMP reduces free cellular Ca, reducing the tension of smooth muscle.

135
Q

What opposes the actions of prostacylin?

A

Thromboxane A2

136
Q

Endothelin

A

Vasoconstrictor

137
Q

Angiotensin converting enzyme (ACE)

A

Found in endothelium cells, it converts ang I to ang II. Plays a role in water retention with ADH. Plays a role in long term water retention and acute response to hemorrage, but not moment to moment regulation.

138
Q

Reactive hyperemia

A

When blood flow is reestablished after a temporary occlusion, blood flow is elevated above its original level. Local metabolites (CO2, H, K, lactic acid, and adenosine) accumulate and act to produce vasodilation until) O2 levels are restored.

139
Q

Active hyperemia

A

Increase in flow beccause of increased metabolic needs of surrounding tissue.

Example: skeletal muscle during exercise

140
Q

Transmural pressure

A

Difference in pressure between two walls

Example: in blood vessel and outside of the vessel

141
Q

Myogenic hypothesis

A

Smooth muscle cells respond to changes in transmural pressure, stretch, by constricting. This keeps flow to a tissue fairly constant when the metabolic needs of the tissue are not changing.

142
Q

Autoregulation

A

Changes in flow without changes in local metabolism. It is the intrinsic ability of the vessel to maintain constant blood flow without changes in perfusion pressure. This impacts the smooth muscle of the vessels.

143
Q

What are methods of extrinsic regulation of blood flow?

A

vasodilation and vasoconstriction in response to neural signals

144
Q

Alpha receptors

A

Constrictor response to catecholamines

Alpha 1: vessels, mediated by inositol triphosphate

Alpha 2: vasoconstrictors by means of reducing uptake of norepi, mediated by reduced cAMP levels

145
Q

B2 receptors

A

dilator response to catetcholamines, mediated by cAMP

146
Q

How do sympathetics affects vasodilation/constriction?

A

Sympathetic action depends on the concentration of receptor types in the region, but predominantly has the impact of constriction. This results in increased blood pressure because of increased vascular resistance in arteries. The veins are also constricted increasing preload on the heart. However, in areas like skeletal muscle, B2 concentration is higher and there is increased blood flow, resulting in readiness for “fight or flight” response.

147
Q

Contrast the sympathetic and parasympathetic innervation of vessels.

A

Sympathetics are present almost all vessles and parasympathetic innervation is rare in vessels except genital organs, salivary glands, and lower GI.

148
Q

What is the role of chemoreceptors in extrinsic regulation of vascular tone?

A

Response to the levels of O2 and CO2 to promote constriction or dilation when needed.

149
Q
A
150
Q

Ejection fraction

A

EJ = SV/EDV

Normally >55%

151
Q

Relate cardiac output to oxygen consumption via equation

A

CO = oxygen consumption(ml/min)/(a-v)

USMLE STEP 1 (15 decks)

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